E-cadherin siRNA促进胃癌SGC7901细胞耐药与增殖

基础医学与临床 ›› 2011, Vol. 31 ›› Issue (9): 1006-1010.

E-cadherin siRNA促进胃癌SGC7901细胞耐药与增殖

陈勇¹,刘巍²,高鸿³

1. 河北医科大学第四医院
2. 河北省石家庄市河北医科大学第四医院肿瘤内科
3.

收稿日期:2010-05-10 修回日期:2010-10-03 出版日期:2011-09-05 发布日期:2011-09-05
通讯作者: 刘巍 E-mail:hebeiliuwei@yahoo.com.cn

E-cadherin siRNA promotes drug resistance formation and proliferation in gastric cancer SGC7901 cell linein gastric cancer SGC7901 cell line

Received:2010-05-10 Revised:2010-10-03 Online:2011-09-05 Published:2011-09-05

摘要/Abstract

摘要： 目的：研究E-cadherin siRNA对胃癌SGC7901细胞化疗敏感性和增殖能力的影响，并对其相关机制进行初步探讨。方法：用Lipofectamine 2000将E-cadherin siRNA及阴性对照序列转入SGC7901细胞，用MTT法检测细胞对药物的敏感性并观察细胞增殖能力。Western印迹法检测细胞E-cadherin、PTEN、AKT、p-AKT、Bax和Bcl-2蛋白表达。结果：SGC7901 细胞转染E-cadherin siRNA后显著抑制细胞E-cadherin蛋白表达 (P<0.05)。转染E-cadherin siRNA后细胞对CDDP、5-FU、Paclitaxel和ADR的IC50分别为：4.375±0.199、6.855±0.780、2.530±0.259和0.368±0.042mg/L；阴性对照组分别为：2.882±0.166、4.058±0.946、1.483±0.225和0.228±0.012mg/L，转染E-cadherin siRNA细胞对CDDP、5-FU、Paclitaxel和ADR的IC50显著高于阴性对照组(P<0.05)。转染E-cadherin siRNA细胞增殖能力显著高于阴性对照组(P<0.05)。转染E-cadherin siRNA 72h后PTEN和Bax蛋白表达显著低于阴性对照组(P<0.05)，而p-AKT和Bcl-2蛋白表达显著高于阴性对照组(P<0.05)。结论：干扰E-cadherin表达导致AKT通路的激活和对凋亡平衡的调控可能是促进SGC7901细胞耐药和增殖的一个机制。

关键词: E-cadherin , 耐药 , 增殖 , PTEN , 凋亡

Abstract: Objective: To explore the effect of E-cadherin siRNA on drug sensitivity and cell proliferation and their related mechanisms in SGC7901 cell line. Methods: SGC7901 cell line was transfected with E-cadherin siRNA by means of Lipofectamine 2000. Drug sensitivity of transfected cells to CDDP、5-FU、Paclitaxel and ADR was tested using MTT assay. And proliferation changes of cells were detected after transfection. Protein changes of E-cadherin, PTEN, AKT, p-AKT, Bax and Bcl-2 were detected by Western blot. Results: The E-cadherin protein expression was significantly decreased after E-cadherin siRNA transfection(P<0.05). The IC50 of CDDP、5-FU、Paclitaxel and ADR in E-cadherin siRNA tansfected group were significantly higher than in negative control group(4.375±0.199mg/L vs 2.882±0.166mg/L, 6.855±0.780mg/L vs 4.058±0.946mg/L, 2.530±0.259mg/L vs 1.483±0.225mg/L, 0.368±0.042mg/L vs 0.228±0.012mg/L respectively, P<0.05). Compared to the control group, cell proliferation was significantly increased in SGC7901 cell transfected with E-cadherin siRNA. The expression of PTEN and Bax protein were significantly lower than the control group 72h after trasfection(P<0.05), while the p-AKT and Bcl-2 protin was higher than the control group (P<0.05). Conclusion: E-cadherin siRNA can activate AKT pathway and regulate apoptotic balance, which may be one of mechanisms on promoting drug resistance and proliferation.

Key words: E-cadherin, Drug resistance, Proliferation, PTEN, Apoptosis

中图分类号:

陈勇刘巍高鸿. E-cadherin siRNA促进胃癌SGC7901细胞耐药与增殖 [J]. 基础医学与临床, 2011, 31(9): 1006-1010.

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